Kaplan Pharm Essentials-Autonomics

Front 1

**M=

Back 1

Parasympathetic + Sweating (sym)

SN: Thermoregulatory is sympathetic anatomically, but parasympathetic physiologically (2 cholinergic synapse)

Front 2

Epi and NE both (+) adrenoreceptors, what is the difference between the two?

Back 2

Epi is carried in blood, while NE is an NT

Front 3

DA (sympathetic NT) activates D1 receptors , which cause ____ in renal & mesenteric bed.

Back 3

Vasodilation

Front 4

Which synapses can you block to reduce reflex bradycardia?

Back 4

Nn ("Ganglionic blocker, block both PANS & SANS)

OR

M2

Front 5

Which pairs of receptors increase & decrease BP, respectively? (useful for cardiac tracing)

Back 5

alpha 1, B2

Front 6

Which pairs of receptors increase & decrease HR, respectively?

Back 6

B1, M2

Front 7

What is a memory trick for M receptors?

Back 7

M1 (head), M2 (tilt head to heart), M3 (everywhere else)

Exception: Eyes=M3

Front 8

**What is special about the M3 receptors in blood vessels?

Back 8

There is no agonists!!! (No innervation and No circulating ACh) -->Physiologically unimportant, but can still functional (eg: M-agonist OD --> HypoTN)

Front 9

Which receptor on vessels control BP at all time and thus have both innervation and blood born signal molecules?

Back 9

Alpha 1 receptor (via NE)

Front 10

Which receptor on vessels decrease BP and only respond to Epi?

Back 10

B2

Front 11

**What is the main receptor difference between M & N receptors?

Back 11

M receptors use G protein

N receptors is direct ion channel

Front 12

Blood vessel and sweat glands are sole innervated by which autonomic system?

Back 12

SANS

Front 13

Which autonomic system predominates GI?

Back 13

PANS

Front 14

If PANS and SANS got into a fight, who is going to win?

Back 14

PANS

Front 15

Which M-agonist is used for ileus and urinary retention?

Back 15

Bethanechol

Front 16

Which M-agonist is used for diagnosis of asthma?

Back 16

Methacholine

Front 17

What is the M-agonist pilocarpine used for?

Back 17

Glaucoma (topical)

Xerostomia (sjogren's)

Front 18

**How do you distinguish myasthenia from cholinergic crisis?

Back 18

Use short acting AChE I edrophonium

Front 19

**What is the structural difference between physostigmine & neostigmine/pyridostigmine?

Back 19

Tertiary Amine (lipid soluble) =Enter CNS

Quarternary amine (+ charge)=DN enter CNS

Front 20

**Physostigmine is used as an antidote to another tertiary amine, known as _____.

Back 20

Atropine

Front 21

**What are neostigmine/pyridostigmine used for?

Back 21

Like bethanechol, act on periphery.
Ileus/Urinary Retention

Myasthenia TREATMENT (diagnosis use edrophonium)

Reversal of non-depolarizing NM blocker

Front 22

Physo VS Pyridostigmine?

Back 22

"Pyro from down below" (pyridostigmine=DN enter CNS)

Front 23

**What AChEI is used for Alzheimer's Dz?

Back 23

Donepezil

Front 24

**Organophosphates are ______ inhibitors of AChEI. All other AChEI are __________.

Back 24

Irreversible


Reversible (competitive)

Front 25

**What are some use of organophosphates?

Back 25

Glaucoma (echothiophate)

Insecticides (mala/parathion)

Nerve Gas (sarin)

Front 26

What is the primary pathology in Alzheimer's Dz?

Back 26

Loss of ACh neuron in Meynert's nucleus

Front 27

What is the classical clue to AChEI poisoning?

Back 27

Dumbbelss (Mostly M3)

Diarrhea
Urination
Miosis
Bradycardia
Bronchoconstriction
Excitation= Exception (mm&CNS/ Nm&M1)
Lacrimation
Salivation
Sweating

Front 28

How do you treat AChEI poisoning?

Back 28

Atropine (for M effect; dn take care of excitation)

Pralidoxime (2-PAM) (Time-dependent regeneration of AChE b/c of loss of functional group that is required for 2-PAM to grab onto)

Front 29

To which kind of drug class does atropine belong?

Back 29

M-receptor antagonist

Front 30

What is the source of atropine?

Back 30

Plants

Belladonna alkaloids (big pupils)
Jimsonweed (hallucination; "Loco seeds"

Front 31

Why is atropine OD so harmful to young kids?

Back 31

Hyperthermia (sweating is blocked --> vasodilation)

Front 32

**What are some drugs with anti-M effect (eg: atropine-like SE)

Back 32

Antihistamine (1st gen)
Tricyclic
Antipsychotics (chlorpromazine, thioridazine)
Quinidine
Amantadine
Meperidine

Front 33

How do you treat acute atropine OD?

Back 33

Symptomatic

+

Physostigmine

Front 34

What are the names of atropine like substances consist of?

Back 34

"trop's" and "scop's"

Front 35

What is ipratropium used for?

Back 35

Asthma/COPD (no CNS entry)

Front 36

What is scopolamine used for?

Back 36

Motion sickness (induce short-term memory loss/sedation)

Front 37

What is benztropine/Trihexyphenidyl used for?

Back 37

Loss of DA (excitatory molecule)=M-antagonist counteract the action of relative increase in ACh

eg: Parkisonism OR
eg: EPS induced by antipsychotics (esp. haloperidol)

Front 38

What are Tolterodine/Oxybutynin used for?

Back 38

Urinary Incontinence

Front 39

What is the only Nicotinic antagonist (ganglion blocker) mentioned?

Back 39

Mecamylamine

Front 40

Why are most ganglion blocker not a/v anymore?

Back 40

Toxicities

Front 41

What is the function of ganglion blocker?

Back 41

Diminish the PREDOMINANT autonimic tone

eg: block CV reflex (PANS predominant) elicited by vasoconstrict/dilation

Front 42

Ganglionic blocker is useful in ______ tracings.

Back 42

Cardiac

eg: Pretx w/ blocke to see if a particular drug is an B1B2 agonist, b/c if u dilate, u get increased HR, and if u increase HR, u get dilate. See which one is predominant.

Front 43

What is the steps of DA synthesis?

Back 43

DA --> DOPA --> DA --> NE

Front 44

Which step of catecholamine synthesis take place inside vesicle?

Back 44

DA --> NE (DA is uptake into vesicle)

Front 45

What are the 4 fates of NE?

Back 45

1. Bind post-synaptic receptor
2. Reuptake
3. Metabolized by COMT/MAO
4. Bind pre-synaptic alpha-2 receptor (Gi)

Front 46

Which drugs increase NE in the synapse?

Back 46

MAOI

Releaser

Reuptake Inhibitor

Front 47

How does MAOI work?

Back 47

Prevent MAO from killing NE in mobile pool (the pool of free NE released from vesicle/reuptake) inside the prejunctional nerve terminal

Front 48

How does releaser work?

Back 48

Displace NE from mobile pool and into synapse

Front 49

**What are 3 releasers of NE?

Back 49

Tyramine (red wine, cheese)

Amphetamines (eg: methylphenidate for ADD)

(Pseudo) Ephedrine

Front 50

A fatal drug interaction, ______ crisis, results from _______ Inhibitor which decrease gut and liver metabolism of tyramine/amphetamine.

Back 50

Hypertensive; MAO-A

Front 51

**What are 2 NE reputake inhibitors?

Back 51

Cocaine

TCA

Front 52

Name an MAOI used to increase NE.

Back 52

Phenelzine

Front 53

How do you decrease NE in synapse?

Back 53

Block RLS

(+) Alpha-2 receptor (negative feedback)

Destroy vesicle

Block exocytosis

Front 54

How do you block RLS in NE synthesis?

Back 54

Methyl-p-tyrosine (block tyrosine hydroxylase)

Front 55

What are two alpha 2 agonist?

Back 55

Clonidine

Methyldopa

Front 56

How do you destroy the vesicle in which NE is made?

Back 56

Reserpine

Front 57

How do you block exocytosis of NE?

Back 57

Guanethidine

Front 58

Guanethidine MOA parallel which inhibitor of ACh release?

Back 58

Botox

Front 59

Which adrenergic receptor is essentiallly the exact opposite of M3?

Back 59

alpha 1

Front 60

Alpha 1 promotes sm. mm _______ everywhere, including the ______ causing urinary retention.

Back 60

contraction; prostate

Front 61

What is a paradoxical effect does alpha 1 have on the kidney?

Back 61

Decrease renin release

Front 62

What does alpha 2 adrenergic receptor do?

Back 62

Negative FB

Decrease insulin release

Front 63

**What is the B1 effect on eyes?

Back 63

Decrease aq. humor production
(Tx: Open angle glaucoma)

Front 64

**What is the B1 effect on kidney?

Back 64

Increase renin

Front 65

**What is special about innervation of B2?

Back 65

NOT INNERVATED = (+) by Epi in blood

Front 66

**B2 is the _______ receptor.

Back 66

Metabolic (Does lots of glycogenolysis/G.Neogenesis)

Front 67

What is B2 effect on sm. mm, including blood vessels, uterus, and bronchioles?

Back 67

Relaxation

Front 68

What does B2 do to skeletal mm?

Back 68

Increase contractility (tremors)

eg: OD on anti-asthmatic drug
eg: Using B-blocker to increase performance

Front 69

How do you remember the B1 vs B2 effects?

Back 69

"1 heart 2 lungs"

"1 heart kid, 2 lungs"

Front 70

What does D1 in the periphery do?

Back 70

Vasodilation (renal, mesenteric, coronary)

Front 71

Which adrenoreceptors have higher sensitivity, Alpha or Beta?

Back 71

Beta

Front 72

When drug exerts both alpha and beta response, _____ predominates in low doses, and _____ predominates in high doses.

Back 72

B, alpha

Front 73

What is the effect of increasing dose of DA?

Back 73

Activation of
D1--->B1--->Alpha1

@ medium dose, B1-->Increase HR
@ high dose, alpha1-->Reflex bradycardia b/c increase TPR

Front 74

Which alpha1 agonist is used as an OTC nasal decongestant?

Back 74

Phenylephrine

SE=Prostate and eye (PE)
Replaced pseudoephedrine (PE)

Front 75

What is the primary use for for alpha2 agonist?

Back 75

Moderate HTN (negative FB on prejct-sympathetic outflow)

Front 76

What are the alpha2 agonists?

Back 76

alpha=MC^2

Methyldopa, Clonidine, alpha2

Front 77

**Which adrenergic receptor is responsible for widening pulse pressure?

Back 77

B1

Front 78

Which B agonist (B1=B2) is used for bronchospasm, heart block, and bradyarrhythmia?

Back 78

Isoproterenol

Front 79

What is dobutamine (B1>B2) used for?

Back 79

CHF (increase CO)

Front 80

What are the Selective B2 agonist used for asthma?

Back 80

LA
-Salmeterol
SA
-Albuterol
-Terbutaline
-Metaproterenol

Front 81

What Selective B2 agonist is used for premature labor?

Back 81

Ritodrine (relax uterus)

Front 82

What is a main SE of B2 agonist?

Back 82

Flushing

Front 83

What drugs produce flushing?

Back 83

Isoproterenol, Vasodilator, Niacin

Front 84

Which drugs cause histamine release?

Back 84

Vancomycin ("Red man syndrome")

Morphine

Amphotericin B

Front 85

**What is the difference between the mixed-acting agonist NE & Epi?

Back 85

NE acts on all adrenergic receptor EXCEPT B2 (B2 not innervated)

Epi acts on A1, A2, B1, AND B2

eg: NE can only increase BP, Epi can Increase/Decrease BP

Front 86

NE is essentially A1B2 agonist, why?

Back 86

A2 effect can largely be ignored b/c it is a FB system

Front 87

What is the effect of NE?

Back 87

Initial tachycardia & HTN, LT reflex bradycardia

Front 88

Why do you need at least 2 picture to describe the dose dependent effect of Epi?

Back 88

Epi can Increase/Decrease BP

Front 89

Low dose Epi || ______ profile; it is _____ dominated.

Back 89

Isoproterenol (B1=B2); Heart

Front 90

High Dose Epi || ______ profile; it is _____ dominated.

Back 90

NE; Vessel

*remember: at high doses, alpha response > beta

Front 91

T/F: B2 has lots of metabolic effect, aimed at raising blood sugar.

Back 91

T

Front 92

**How do we differential between high-dose Epi VS NE?

Back 92

Epinephrine Reversal (Give A1 blocker, if it is Epi then transition from HTN --> HypoTN will result from unmasking of B2 receptors)

Front 93

What is the emergency use of Epi?

Back 93

Anaphylaxis

Asthma

Front 94

What is the main tx for pheochormocytoma?

Back 94

Non-selective Alpha blocker (Phenoxybenzamine, a noncompetitive inhibitor)

"Pheno for Pheo"

Front 95

What are the Alpha1 selective blockers?

Back 95

"Zosin": Alpha1, Tx HTN

"Osin": Alpah1A, Tx BPH ONLY

Front 96

What class of drug does Yohimbine belong to?

Back 96

A2 blocker, used for postural hypoTN & impotence.

Front 97

What makes A2 blocker Mirtazapine special?

Back 97

It has a unique MOA (raises NE level)

Front 98

Why does non-selective Alpha blocker give > reflex tachycardia than A1 selective blocker?

Back 98

A2 negative FB is blocked

Front 99

Why must you taper the dose of BB slowly during withdrawal?

Back 99

Receptor upregulation during chronic use --> rebound tachycardia

Front 100

B1 receptors are ______-selective.

Back 100

Cardio

Front 101

B1 w/ intrinsic sympathomimetic activity (ISA=partial agonist) have what kind of advantage?

Back 101

It does not increase lipid level
(eg: Acebut/Pind-olol)

Front 102

**a-m -olol= ______ only
n-z -olol= _____

Back 102

B1

Non-selective

Front 103

**What are the 2 significant SE of B2, blockade (the "metabolic" receptor)?

Back 103

Hypoglycemia (Ppt DM)

Increase LDL/TG

Front 104

**Non-selective BB is CI in which 2 types of pts?

Back 104

DM

Asthmatics

Front 105

What is the tx of BB overdose?

Back 105

Glucagon (acts through separate receptor from adrenergic receptor to increase cAMP)

Front 106

Timolol is used primarily for what?

Back 106

Galucoma

Front 107

Propanolol is used to tx ________ ______.

Back 107

Essential tremor (hyperstimulated B2)


*Rem B2 causes contractility/tremor in skeletal mm

Front 108

Any BB w/ -ilol or -alol means what?

Back 108

BB + Other activity

Front 109

LAbetalol and CArvedilol have both ___ & B blocking activity, and is used for the tx of _______.

Back 109

Alpha1; CHF (they both lower BP)

Front 110

Sotalol also have what kinda of activity at allows it to be used as class III antiarrhytmic?

Back 110

K+ blocker

Front 111

What are 4 classes of drugs used to tx glaucoma?

Back 111

Increased Outflow
-Cholinomimetics ((+) M receptor --> ciliary mm contraction)
-Carbonic Anhydrase Inhibitor


Decrease Aq. Humor Production
-BB (B1 block--> Decrease Synthesis)
-Osmotic Diuretic (Mannitol)

Front 112

What is the primary cholinomimetic used to tx glaucoma?

Back 112

Pilocarpine

Front 113

What is the CAI used for glaucoma?

Back 113

Acetazolamide